heme 3 Flashcards
Vitamin K deficiency labs
PT + INR prolonged + PTT normal or mildly prolonged (prolonged with severe vitamin k deficiency) + inciting factor
what is d-dimer?
fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis
Other reasons for elevated d-dimer
any acute or inflammatory process (eg, age >50 years, recent surgery or trauma, acute illness, pregnancy or postpartum state, rheumatologic disease, renal dysfunction [estimated glomerular filtration rate <60 mL/min/1.73 m2]), sickle cell disease, pulmonary disease
life span of one red blood cell
120 days
effect of prophylactic heparin on PTT
small, but significant, increase in aPTT (mean 38.6)
lab profile of factor VIII deficiency
Prolonged PTT
Effect of warfarin on PT and PTT
Typically prolongs the PT alone, but at high levels can prolong both tests.
Effect of heparin on PT and PTT
Heparin typically prolongs the aPTT alone (because PT reagents contain heparin-binding agents that block heparin effect), but at high levels heparin can prolong both tests.
Effect of direct thrombin inhibitors on PT and PTT
typically prolong both tests
Effect of Xa inhibitors on PT and PTT
prolong the PT and aPTT, although these effects are variable
Effect of liver disease on PT and PTT
Typically prolongs just PT, but also prolong PTTs in severe liver disease
Describe the clotting cascade
https://upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Coagulation_full.svg/400px-Coagulation_full.svg.png
what is a lupus anticoagulant (pathophys)
- Acquired autoantibody to phospholipids. Interacts with platelet membrane phospholipids, increasing adhesion and aggregation of platelets, which accounts for in vivo prothrombotic characteristics.
- misnomer, as it is actually a prothrombotic antibody.
Initial workup of prolonged PTT
Step 1 = Mixing study →
IF corrects = deficient clotting factor
IF remains abnormal = inhibitor present (ie lupus anticoagulant)
confirm presence with prolonged phospholipid-sensitive functional clotting testing (dilute Russell’s viper venom time, or the Kaolin clotting time)
Concept of a mixing study
You’re looking for an inhibitor in plasma or a deficient clotting factor. Patient’s plasma is mixed with normal pooled plasma and the clotting is reassessed. If a clotting inhibitor such as a lupus anticoagulant is present, the inhibitor will interact with the normal pooled plasma and the clotting time will remain abnormal. However, if the clotting time of the mixed plasma corrects towards normal, the presence of an inhibitor such as the lupus anticoagulant is excluded, and instead a deficient quantity of clotting factor (that is replenished by the normal plasma) is likely.
treatment of lupus anticoagulant
IF history of thrombosis + documented history of lupus anticoagulant twice → consider indefinite AC
IF no history of thrombosis → observation
Prevalence of lupus anticoagulant
Relatively common (believed to be approximately 5% in adults, with a predominance among females of reproductive age).
Why does renal disease cause coagulopathy
uremic platelet dysfunction
Reversal agent for Xa inhibitors
Andexxa
Problem with Xa inhibitor reversal agent
Not available on most pharmacy formularies
Thrombotic risk of liver disease
Cirrhotics are coagulopathic but also hypercoagulable (protein c and s deficiency). This is why they still need heparin dvt ppx (from studies).
Only case in which hypercoagulability workup would change management
High risk anti phospholipid syndrome, which requires coumadin
Where are platelets produced?
Bone marrow, just like red and white cells.
What is “treatment failure” from NOACs typically due to?
Nonadherence – patients missing doses. Due to short half life, you are at increased thrombotic risk by just missing a dose or two.
